Objective We investigated the clinical features and the potential risk factors of malnutrition in patients with chronic heart failure(CHF),and constructed the risk prediction model of malnutrition.Methods A total of459 CHF patients admitted between January 2023 and July 2024 were classified into a normal nutrition group and a malnutrition group based on the geriatric Nutrition Risk Index(GNRI)score upon admission.The patient-related data were gathered,and single-variable and multi-variable logistic analyses were first carried out to identify the risk factors associated with the malnutrition risk.Subsequently,the stepwise regression approach was employed to define the inclusion criteria and construct a malnutrition nomogram model for CHF patients.The diagnostic efficacy and calibration of this model were appraised using the ROC curve and calibration curve,and its clinical utility was assessed via the clinical decision curve.A P value less than 0.05 signified statistically significant differences.Results Anxiety(OR=1.1902,95%CI:1.0217～1.3865),urea nitrogen(OR=1.4842,95%CI:1.1187～1.9691),low body weight(OR=0.8463,95%CI:0.7852～0.9121),and low albumin(OR=0.0467,95%CI:0.0172～0.1268)were risk factors for malnutrition.The optimal model inclusion factors were selected by stepwise regression,including:Body weight,7 items of Generalized Anxiety Disorder Scale(GAD-7),urea nitrogen,uric acid,albumin,total cholesterol,high density lipoprotein cholesterol(HDL-L),low density lipoprotein cholesterol(LDL-L),D-dimer.The area under the ROC curve(AUC)of the column chart model based on the above factors is 0.996(95%CI:0.971～0.978),with a sensitivity of 97.8%and a specificity of 97.1%.The C-index validated internally in the calibration curve was 0.824.The calibration chart and validation results demonstrate good consis-tency and applicability.Conclusion The column chart prediction model created in this study based on nine factors including body weight,GAD-7,urea nitrogen,uric acid,albumin,total cholesterol,HDL-L,LDL-L,and D-dimer had good calibration and prediction performance,and had good clinical practicality,which was helpful for clinicians to make diagnosis and treatment decisions for malnutrition in CHF patients.

Thoracolumbar trauma, including fractures, dislocations and spinal cord injuries, often result from high-energy injuries such as traffic accidents and falls from heights. It not only causes severe pain and restricted movement for patients, but also leads to neurological damage and even permanent disability. Currently, the diagnosis and treatment of thoracolumbar trauma are faced with many problems, such as possible missed diagnosis and misdiagnosis, lack of individualized and standardized treatment plans, and lack of objective and quantitative metrics for postoperative assessment. Artificial intelligence (AI) technology offers innovative ideas to these problems. Among them, the core AI technology such as machine learning (ML), deep learning (DL), computer vision, and robotics has demonstrated outstanding capabilities in medical image analysis, clinical decision support, etc., which can significantly improve the diagnostic precision, surgical planning efficiency, and postoperative management level of thoracolumbar trauma. At present, application of AI technology in cross-modal data integration, clinical decision support, and long-term efficacy prediction in the field of thoracolumbar trauma remains to be systematically sorted out. To this end, the authors reviewed the research progress of AI technology in the diagnosis, treatment, and postoperative management of thoracolumbar trauma, providing a reference for a wide application of AI technology in the management of thoracolumbar trauma.

Thoracolumbar trauma, including fractures, dislocations and spinal cord injuries, often result from high-energy injuries such as traffic accidents and falls from heights. It not only causes severe pain and restricted movement for patients, but also leads to neurological damage and even permanent disability. Currently, the diagnosis and treatment of thoracolumbar trauma are faced with many problems, such as possible missed diagnosis and misdiagnosis, lack of individualized and standardized treatment plans, and lack of objective and quantitative metrics for postoperative assessment. Artificial intelligence (AI) technology offers innovative ideas to these problems. Among them, the core AI technology such as machine learning (ML), deep learning (DL), computer vision, and robotics has demonstrated outstanding capabilities in medical image analysis, clinical decision support, etc., which can significantly improve the diagnostic precision, surgical planning efficiency, and postoperative management level of thoracolumbar trauma. At present, application of AI technology in cross-modal data integration, clinical decision support, and long-term efficacy prediction in the field of thoracolumbar trauma remains to be systematically sorted out. To this end, the authors reviewed the research progress of AI technology in the diagnosis, treatment, and postoperative management of thoracolumbar trauma, providing a reference for a wide application of AI technology in the management of thoracolumbar trauma.

Objective We investigated the clinical features and the potential risk factors of malnutrition in patients with chronic heart failure(CHF),and constructed the risk prediction model of malnutrition.Methods A total of459 CHF patients admitted between January 2023 and July 2024 were classified into a normal nutrition group and a malnutrition group based on the geriatric Nutrition Risk Index(GNRI)score upon admission.The patient-related data were gathered,and single-variable and multi-variable logistic analyses were first carried out to identify the risk factors associated with the malnutrition risk.Subsequently,the stepwise regression approach was employed to define the inclusion criteria and construct a malnutrition nomogram model for CHF patients.The diagnostic efficacy and calibration of this model were appraised using the ROC curve and calibration curve,and its clinical utility was assessed via the clinical decision curve.A P value less than 0.05 signified statistically significant differences.Results Anxiety(OR=1.1902,95%CI:1.0217～1.3865),urea nitrogen(OR=1.4842,95%CI:1.1187～1.9691),low body weight(OR=0.8463,95%CI:0.7852～0.9121),and low albumin(OR=0.0467,95%CI:0.0172～0.1268)were risk factors for malnutrition.The optimal model inclusion factors were selected by stepwise regression,including:Body weight,7 items of Generalized Anxiety Disorder Scale(GAD-7),urea nitrogen,uric acid,albumin,total cholesterol,high density lipoprotein cholesterol(HDL-L),low density lipoprotein cholesterol(LDL-L),D-dimer.The area under the ROC curve(AUC)of the column chart model based on the above factors is 0.996(95%CI:0.971～0.978),with a sensitivity of 97.8%and a specificity of 97.1%.The C-index validated internally in the calibration curve was 0.824.The calibration chart and validation results demonstrate good consis-tency and applicability.Conclusion The column chart prediction model created in this study based on nine factors including body weight,GAD-7,urea nitrogen,uric acid,albumin,total cholesterol,HDL-L,LDL-L,and D-dimer had good calibration and prediction performance,and had good clinical practicality,which was helpful for clinicians to make diagnosis and treatment decisions for malnutrition in CHF patients.

AIM:To investigate the impact of aquaporin 4(AQP4)expression inhibition on autophagy and apoptosis in a mouse model of cerebral ischemia-reperfusion(I/R)injury,and to elucidate its underlying mechanism.METHODS:Cerebral I/R injury was induced in mice via transient middle cerebral artery occlusion(tMCAO).Totally 60 mice were randomly divided into sham group,I/R group,AQP4 inhibition group,and 3-methyladenine(3-MA)group,with 15 mice in each group.Among them,the mice in sham and I/R groups received intraperitoneal injections of normal saline,while those in AQP4 inhibition group and 3-MA group received intraperitoneal injections of AER-271(2 mg·kg-1·d-1)and AER-271+3-MA(2 mg·kg-1·d-1)for 3 d,respectively,once per day.Longa score was adopted to assess the neu-rological function,and to record changes in body weight.Cerebral infarction volume and histopathological alterations were evaluated using hematoxylin-eosin staining.Western blot analysis was performed to determine the levels of AQP4,LC3-Ⅱ,P62 and cleaved caspase-3,while the LC3-Ⅱ,P62,cleaved caspase-3 and NeuN(neuronal marker)colocalization and expression assessment were conducted with immunofluorescence.RESULTS:The mice in I/R and AQP4 inhibition groups exhibited extensive cerebral infarction,cerebral edema,and elevated Longa scores.However,in comparision to I/R group,the mice in AQP4 inhibition group showed significantly reduced cerebral infarct volume,cerebral edema vol-ume,and Longa score(P<0.05).Additionally,in contrast to sham group,the mice in I/R group displayed increased ex-pression of AQP4,LC3-Ⅱ and cleaved caspase-3(P<0.01),accompanied by decreased body weight and P62 expression(P<0.05 or P<0.01).Furthermore,compared with I/R group,the mice in both AQP4 inhibition group and 3-MA group demonstrated a decrease in the expression levels of AQP4,LC3-Ⅱ and cleaved caspase-3(P<0.05 or P<0.01),along with increased body weight and P62 expression(P<0.05 or P<0.01).Nonetheless,no significant differences were ob-served between AQP4 inhibition group and 3-MA group regarding Longa score,cerebral infarct volume,body weight,and the expression of AQP4,LC3-Ⅱ,cleaved caspase-3 and P62.CONCLUSION:Inhibition of AQP4 expression signifi-cantly reduces cerebral infarction area and nerve injury severity in tMCAO mice.Moreover,AQP4 expression inhibition decelerates autophagy and apoptosis after cerebral infarction,with the additional autophagy inhibitor showing no notable impact on the protective effect of AQP4 inhibition.

Objective:To analyze the influence of vitamin D 3 supplementation on the clinical efficacy of mesalazine in patients with ulcerative colitis (UC). Methods:From January 2015 to December 2020, patients with mild-to-moderate active UC were retrospectively and continuously enrolled, who accepted mesalazine treatment for at least 12 months at the Second Affiliated Hospital of Wenzhou Medical University. According to simultaneous supplement of vitamin D 3 (125 IU/d), the patients were divided into study group and control group. Demographic and disease characteristics, serum 25-hydroxyvitamin D[25(OH)D] levels and other information were collected through retrieving hospital database. Student′s t-test, Mann-Whitney U test and Chi-square test were applied for comparison of disease characteristics. The changes of modified Mayo scores[ΔMayo] and 25(OH)D[Δ25(OH)D] were compared before and after treatment by paired t-test, Wilcoxon signed rank test and Chi-square test. Multiple linear regression model was used to analyze the independent factors affecting ΔMayo and Δ25(OH)D, and variables with P-values less than 0.20 in the univariate analysis were allowed for further multivariate analysis. Results:A total of 74 UC patients (44 males, 30 females), with median age (range) 39.5 (20-76) years old, were analyzed and respectively assigned into study group ( n=36) and control group ( n=38). In study group, the average level of serum 25(OH)D was significantly increased at month 12 compared with that at baseline [(22.87±7.30) μg/L vs. (18.15±7.48) μg/L, P<0.001]. However, no significant elevation of serum 25(OH)D was found in control group [(19.17±8.49) μg/L vs. (19.82±9.47) μg/L, P=0.466]. Furthermore, there was a significant decrease of modified Mayo score [-3(-4.75, -1.25) vs.-2(-3.25, 0), P=0.034] and a higher clinical remission rate (55.6% vs. 28.9%, P=0.020) at month 12 in study group than those in control group. In addition, according to the baseline level of serum 25(OH)D before mesalazine treatment, 74 UC patients were divided into vitamin D deficiency group ( n=38, serum 25(OH)D<20 μg/L) and non-deficiency group ( n=36, serum 25(OH)D≥20 μg/L). At month 12 in vitamin D deficiency group, patients with vitamin D3 supplementation had a greater decline in modified Mayo score [-4(-5.75, -2) vs.-2(-4, 0), P=0.048] and a higher clinical remission rate (60.0% vs. 22.2%, P=0.019) compared with those without. Conclusions:In patients with mild-to-moderate active UC receiving mesalazine treatment, vitamin D3 supplementation may improve the clinical efficacy, especially in patients with vitamin D deficiency.

Objective To investigate the effect of ultrasound?guided transversus abdominis plane block after general anesthesia induction on cyclic stress and postoperative analgesia in patients treated with abdominal surgery. Methods Sixty patients scheduled for elective abdominal surgery were divided into 2 groups with 30 cases in each. All were treated with ultrasound?guided transversus abdominis plane block after general anesthesia induction, and 30 cases in observation group received ropivacaine ,while those in control group saline. Anesthesia maintained by propofol combined with remifentanil during surgery ,and postoperative analgesia by sufentanil. The effect of anesthesia and operation were compared. Results Compared with control group,observation group needed less time for analepsia (P < 0.05) ,and there were lower blood pressure and heart rate at 2 min after skin incision and immediately after surgery (P < 0.05). Less propofol and remifentanil were needed in surgery and less sufentanil after surgery in observation group (P < 0.05). The VAS pain score was lower 1 h,4 h,8 h and 12 h after surgery (P < 0.05) ,and there were less times for pressing analgesic pump (P < 0.05). Patients in observation group had higher comfort degree after surgery (P<0.05). Conclusion Ultrasound?guided transversus abdominis plane block after general anesthesia induction is helpful to reduce intraoperative anesthesia used for anesthesia maintenance , and can improve patients′comfort after surgery.

Objective To study the analgesic effect of repeated hyperbaric oxygen (HBO) exposures and explore the mechanism involving neural nitric oxide synthase ( nNOS), nitric oxide ( NO) and γ-aminobutyric acid (GABA).Methods The animal pain model was established and the animals were randomly divided into the HBO group, the hyperbaric air ( HBA) group, the normobaric air (NBA) group and the normobaric oxygen ( NBO) group, and were exposed repeatedly to either HBO or air .The chamber was ventilated with 100％ O2 for 5 min, then, the chamber was pressurized to 0.35 MPa at a rate of 0.10 MPa/min.At the pressure of 0.35 MPa, the chamber was again ventilated with oxygen /air for 60 minutes, and then, was decompressed at a rate of 0.10 MPa/min.The animals were exposed in the chamber one session a day for a succession of 4 days.Analgesic effect was evaluated by abdominal contraction test , and nitrate reductase assay was used to determine the expression levels of NO and NOS in the brain tissue and the spinal cord.NOS inhibitors were given by i.c.v injection to measure the effect of NOS on the analgesic effect of HBO.The nNOS + neurons and glatamic acid decarboxylase ( GAD) positive ( GAD +) neurons in the periaqueductal gray ( PAG) were labeled by fluorescopy.Results Repeated HBO treatment induced a biphasic analgesic effect, including: (1) early analgesia which was displayed an hour after HBO exposure and lasted for about 8 hours; (2) late analgesia which was displayed one day after HBO exposure , reached peak one week later and lasted for about 3 weeks.Three hours after the termination of last HBO exposure , medication of the non-specific NOS inhibitor N′-Nitro-L-arginine-methyl ester hydrochloride ( L-NAME ) and nNOS inhibitor S-methyl-L-thiocitrulline (SMTC) could obviously inhibit early analgesic effect .L-NAME and SMTC could significantly inhibit late analgesia .One hour after HBO exposure, the levels of NO and nNOS in the brain tissue and spinal cord were considerably elevated .The late analgesic effect of HBO significantly decreased , when CGP35348 was injected in the lateral ventricle 7 days after HBO treatment.Immunofluorescence indicated that there was a co-localization between nNOS + neurons and GAD + neurons in the PAG.Conclusions Repeated 4 HBO exposures induced a double -phased analgesia.Initial analgesic effect displayed one hour after HBO treatment, involving activation of nNOS, while late analgesic effect emerged one day after HBO exposure , with the interaction between nNOS and GABA B receptors.

Objective To study the analgesic effect of repeated hyperbaric oxygen (HBO) exposures and explore the mechanism involving neural nitric oxide synthase ( nNOS), nitric oxide ( NO) and γ-aminobutyric acid (GABA).Methods The animal pain model was established and the animals were randomly divided into the HBO group, the hyperbaric air ( HBA) group, the normobaric air (NBA) group and the normobaric oxygen ( NBO) group, and were exposed repeatedly to either HBO or air .The chamber was ventilated with 100％ O2 for 5 min, then, the chamber was pressurized to 0.35 MPa at a rate of 0.10 MPa/min.At the pressure of 0.35 MPa, the chamber was again ventilated with oxygen /air for 60 minutes, and then, was decompressed at a rate of 0.10 MPa/min.The animals were exposed in the chamber one session a day for a succession of 4 days.Analgesic effect was evaluated by abdominal contraction test , and nitrate reductase assay was used to determine the expression levels of NO and NOS in the brain tissue and the spinal cord.NOS inhibitors were given by i.c.v injection to measure the effect of NOS on the analgesic effect of HBO.The nNOS + neurons and glatamic acid decarboxylase ( GAD) positive ( GAD +) neurons in the periaqueductal gray ( PAG) were labeled by fluorescopy.Results Repeated HBO treatment induced a biphasic analgesic effect, including: (1) early analgesia which was displayed an hour after HBO exposure and lasted for about 8 hours; (2) late analgesia which was displayed one day after HBO exposure , reached peak one week later and lasted for about 3 weeks.Three hours after the termination of last HBO exposure , medication of the non-specific NOS inhibitor N′-Nitro-L-arginine-methyl ester hydrochloride ( L-NAME ) and nNOS inhibitor S-methyl-L-thiocitrulline (SMTC) could obviously inhibit early analgesic effect .L-NAME and SMTC could significantly inhibit late analgesia .One hour after HBO exposure, the levels of NO and nNOS in the brain tissue and spinal cord were considerably elevated .The late analgesic effect of HBO significantly decreased , when CGP35348 was injected in the lateral ventricle 7 days after HBO treatment.Immunofluorescence indicated that there was a co-localization between nNOS + neurons and GAD + neurons in the PAG.Conclusions Repeated 4 HBO exposures induced a double -phased analgesia.Initial analgesic effect displayed one hour after HBO treatment, involving activation of nNOS, while late analgesic effect emerged one day after HBO exposure , with the interaction between nNOS and GABA B receptors.

Objective To explore whether hypertonic saline would partake in regulating Notch signaling in microglia in experimentally induced cerebral ischemic rats.Methods Male SD rats were randomly divided into sham group, cerebral ischemia group, normal saline group ( NS group ) , 10%hypertonic saline group (10%HS group) , the model of cerebral ischemia were established in all rats except the sham group by using middle cerebral artery occlusion ( MCAO) .After 2 hours of MCAO, the rats were through reperfusion for 24 h.In addition, rats in the normal saline group and 10% HS group were respectively treated with a continuous intravenous injection of normal saline (0.3 mL/h) and 10%HS (0.3 mL/h) by tail vein for 24 h.Immunofluorescence methods, RT-PCR and Western blot were used to detect the expression of Notch1 and intracellular Notch receptor domain ( NICD) .All data was analyzed by one-way analysis of variance ( ANOVA) , The intergroup comparisons were analyzed by the least-significant-difference (LSD) tests.Differences were considered statistically significant if P<0.05.Results Immunofluorescence showed that the expression of Notch1 and NICD were significantly increased in the microglia around peri-ischemia area in cerebral ischemia group and normal saline group compared to sham group;the expression of Notch1 and NICD in the microglia around peri-ischemia area were significantly reduced in 10% HS group compared to ischemia group and NS group.RT-PCR showed that the mRNA expression of Notch1 was significantly increased in ischemia group and NS group compared to sham group ( sham group: 1.000 ± 0.076; ischemia group: 2.203 ±0.283; NS group: 1.616 ±0.185; P <0.01 ); however, it was significantly reduced in 10% HS group compared to ischemia group and NS group ( ischemia group:2.203 ±0.283; NS group: 1.616 ±0.185; 10%HS group: 1.202 ±0.177; P <0.05 ) .Western blot showed that the protein expression of Notch1 was significantly increased in ischemia group and NS group compared to sham group ( sham group: 0.290 ±0.079; ischemia group: 0.750 ±0.029; NS group:0.765 ±0.182;P<0.01);but was significantly reduced in 10%HS group compared to ischemia group and NS group ( ischemia group:0.750 ±0.029; NS group:0.765 ±0.182;10%HS group:0.390 ±0.195;P<0.05 ) .The protein expression of NICD was significantly increased in ischemia group and NS group compared to sham group ( sham group: 0.401 ±0.196; ischemia group: 0.906 ±0.359; NS group:0.847 ±0.153;P<0.01);but was significantly reduced in 10%HS group compared to ischemia group and NS group ( ischemia group:0.906 ±0.359; NS group:0.847 ±0.153;10%HS group:0.561 ±0.165;P<0.05 ) .Conclusion Our results suggest that HS markedly suppresses Notch signaling in microglia around the ischemia tissue area in experimental induced cerebral ischemic rats.